REB Renal Flashcards
what part of the nephron is involved in converting vitamin D to active form
PCT
what organ produces erythropoietin
kidney
what is the renal capsule
tuft of capillaries and bowman’s capsule
where does ultrafiltration take place
glomerulus
ultrafiltration is dependant on
string hydrostatic pressure in the nephron
approximately how much filtrate is formed everyday?
180L
how much filtrate is excreted in urine?
1.5L
how much filtrate is reabsorbed?
178.5L
how much water, glucose and salt is reabsorbed (%)?
water - 99
glucose - 100
salt - 99.5
Reabsorption of which of the following are active and which are passive water glucose amino acids na cl
passive
cl
water
active
glucose
amino acids
na
What is the passage of substances which are are reabsorbed in the kidney?
Lumen to cells to ECF
What is the passage of tubular secretions?
Peritubular capillaries to tubular lumen
What’s molecules are involved in tubular secretion and what is the importance of this process?
H+, K+, organic ions, wastes
Important for removal of waste and maintaining blood pH by secreting H+ and NH4+
How much urine is formed per min?
1 ml/min
What is the typical pH of urine?
Six
What does substances are commonly found in urine?
Water urea creatinine ions phenol
Outline the blood supply to the glomerulus
Renal - interlobular - arcuate - interlobular - afferent
What is a normal BP range? (MAP)
MAP - 80-180 mmHg
How is the afferent arteriole affected by changes in arterial pressure?
Why is this important?
Changes in arterial pressure or matched by a corresponding change and afferent arteriole resistance
This maintains a constant flow rate
What are the types of intrinsic regulation of renal blood flow?
myogenic
Tubuloglomerular feedback
What is myogenic regulation of renal blood flow?
Stretch of walls of afferent arteriole followed by reflexed contraction of smooth muscle which increases pressure and stretch –> activates nonselective cation channels in smooth muscles –> Ca2+ depolarises
In myogenic regulation of renal blood flow, what cation channels are activated and cause depolarisation?
Calcium
Where are macula densa cells found?
At the junction between the ascending loop of Henle and the distal convoluted tubule
Macular densa sells changes tone in response to
Changes in the rate of blood flow
When there is an increased glomerular filtration rate, there is an increase in the delivery of which ions to the macula densa?
Sodium and chloride
What paracrine agents does the macula densa release?
ATP and adenosine (to increase GFR)
NO ( to decrease GFR)
How do macula densa cells increase tone?
increased pressure –> increased glomerular filtration rate –> increased Na+/Cl- delivery to macula densa –> activates non-selective cation channels –> macula densa to releases paracrine agents such as ATP and adenosine –> increases the tone of afferent arterioles
How do you glomerular capillaries maintain GFR
They are fragile
COOL!
Can GFR be extrinsically controlled?
No
explain extrinsic control of renal blood flow?
1.nerves - sympathetic fibres
noradrenaline –> constriction –> decreases GFR
2.hormones - the vascular smooth muscle cells are sensitive to adrenaline and angiotensin II
the release of what neurotransmitter decreases GFR
noradrenaline
how is renal blood flow controlled at rest?
autoregulation only
how is renal blood flow controlled during severe exercise?
sympathetic NS
adrenaline
–> cause constriction
how is renal blood flow controlled if there is a hemorrhage?
heavy SNS activity
adrenaline
–> reduces fluid loss in urine
how is renal blood flow controlled if there is a long hemorrhage?
NO2 and prostaglandins (PGE2, PGI2) released by macula densa cells
what is the effect of a long-term hemorrahage?
renal ischemia –> hypoxia –> tubular necrosis
how much plasma entering the nephron is filtered in bowman’s capsule
20%
what factors influence glomerular filtration (3) and give their values
- glomerular capillary pressure - 55mm Hg
- plasma colloid osmotic pressure - 30 mmHg
- bowman’s capsule hydrostatic pressure - 15 mmHG
what is the net filtration pressure?
10 mmHg
Creatinine come from _____ which is stored in _____ and synthesised from _____ in the ______ for quick bursts of energy.
Creatinine is formed spontaneously by ______ at a constant rate of ___% and its level depends on _____.
It composes ___% of the nitrogenous component of urine
creatine
skeletal muscles
arginine
liver
phosphocreatine
2%
muscle mass
4%
what conditions change GFR
- alterations in the forces:
- decrease in plasma protein –> increases GFR
- urinary tract blockage –> decreases GFR and increases pressure in bowman’s capsule
- diarrhea –> increased plasma colloid –> decreased GFR - autoregulation and extrinsic control
how does a decrease in plasma protein affect GFR
increases GFR
how does a urinary tract blockage affect GFR and p in the BC
decreases GFR and increases pressure in bowman’s capsule
how does diarrhea affect GFR
increased plasma colloid –> decreased GFR
compare the value of osmolarity in the renal corpuscle and in plasma
same - 300 mosm/L
what is the pH of the filtrate in the renal corpuscle
6
what part of the nephron has cuboidal epithelial cells?
PCT
thick limb LoH
what part of nephron has microvilli?
PCT
what part of nephron has squamous epithelium
thin LoH
what part of nephron has a lot of mitochondria?
PCT
thick limb LoH
function of microvilli
increase reabsorption
what does water move through in the nephron?
tight junctions
aquaporins
the PCT and thin descending limb have what type of aquaporin?
1
the DCT and collecting tubules have what type of aquaporin?
2 (3,4)
what aquaporins are mediated by ADH?
2 (3,4)
are all aquaporins bidirectional?
yup!
are the Na/K pumps located on the basal or apical membrane?
basal
the apical membrane borders the _____ whilst the basal membrane borders the ____
lumen
ECF
what % of the following is reabsorbed in the PCT glucose aa HCO3- phosphate Na K H2O urea lactate
100%
glucose
aa
HCO3- 90%
phosphate - 85%
70%
Na
K
H2O
50%
urea
lactate
where does NaCl reabsorption occur
early PCT
late PCT
what transporters are involved in the reabsorption of NaCl?
early PCT
Na/organic solute cotransporter
Na/H exchanger
**impermeable to CL-
Late PCT
only Na/H exchanger
where is this transporter found:
Na/organic solute cotransporter
early PCT
where is this transporter found:
Na/H exchanger
early PCT
Late PCT
the early PCT is impermeable to
Cl-
how Cl get through the late PCT?
passively diffuses through paracellular pathway
where does glucose reabsorption occur
early PCT
what transporters are involved in the reabsorption of glucose?
SGLT2 cotransporter (na and glucose in) exit through GLUT 2 (1 way)
which transporter is a target for diabetic medications to lower glucose level?
SGLT2 cotransporter
all glucose is reabsorbed until maximum (Tmg) of
2 mmol/min
** 3 times the normal amount
where does protein reabsorption occur?
**only some enters filtrate
PCT
how is protein reabsorbed in the PCT?
through receptor-mediated endocytosis where they are digested by lysosomes into AA
where does AA reabsorption occur?
**either directly from glomerular filtration through digestion of protein by lysosomes or through peritubular blood
early PCT but if there is a lot in the filtrate, it can occur throughout PCT
what transporters are involved in the reabsorption of AA?
Na/aa cotransporter
they exit through different separate passive channels on basal membrane
can HCO3- cross the apical membrane?
NOPE
explain the reabsorption of HCO3-
HCO3- combines with H+ (which are secreted by Na/H exchangers) to produce H2CO3 which is then broken down into H2O and CO2 by carbonic anhydrase
CO2 and H2O enter passively and then recombine to form HCO3- and H+
HCO3- leaves through the HCO3/Na symporter (basal)
what reaction is catalysed by carbonic anhydrase
H2CO3 –> H2O and CO2
explain organic ion secretion in the PCT include the transporters
secretion –> body –> lumen
this the main method for transporting wastes and drugs
this occurs through MDR1 (multidrug) or Na/K-dependant transport
HCO3- leaves through the
HCO3/Na symporter (basal)
what is Fanconi syndrome
disease of PCT dysfunction
Fanconi syndrome is characterised by
excess loss of glucose, aa, phosphate, HCO3- into urine
this leads to acidosis and dehydration
Fanconi syndrome is treated by
hydration and supplements
what the 3 divisions of the LOH
Thin descending
thin ascending
thick ascending
what is the main function of the LoH
maintenance of the highly concentrated medulla and reabsorption of water
osmolarity varies from ____ to ___ in the LoH to _____ in the DCT
300 mosm/L
1200
100
the thin descending LoH has a low permeability to _____ but high permeability to _____
solutes
water
what happens to [filtrate] as water is reabsorbed in the LoH
the filtrate becomes more concentrated
the thin ascending LoH has a impermeable to _____ but permeable to _____
water
solutes
what happens to [filtrate] as NaCl is reabsorbed in the thin ascending LoH
the filtrate becomes less concentrated
what is reabsorbed in the thin ascending LoH
NaCl
the thick ascending LoH actively reabsorbs what ions
na
k
cl
what transporters are involved in the reabsorption of ions in the thick ascending LoH
NKCC2
how do the reabsorbed ions from the thick ascending LoH exit the nephron
cl and k through basolateral transporters
na through the Na/K pump
some K leaks back into the cell through the apical membrane
what is the effect of K+ leaking into the lumen
positive lumen –> cation absorption via tight junction
how do loop diuretics work
inhibiting the NKCC2 transporter in the thick ascending LoH which inhibits salt reabsorption and increases water excretion
what patients use loop diuretics
suffer from renal insufficiency or severe edema
in the early DCT, Na+ enters the apical membrane through
Na/Cl transporters
or NCC
the early DCT reabsorbs ____ but not ____.
how does it affect [filtrate]?
NaCl
water
filtrate is dilute
what hormone acts at the DCT to cause calcium reabsorption
parathyroid hormone
explain calcium reabsorption in the early DCT (include transporter)
enters apical site through facilitated diffusion and exits through the 3Na/Ca exchanger at the basolateral membrane
what are the 2 types of epithelial cells in the late DCT and the CD? what do they control?
principal cell - NaCl transport
intercalated cells - acid/base balance
in principal cells, Na+ is reabsorbed through ___ channels and _____
NCC
ENaC (electrogenic)
ENaC is under the control of
aldosterone
what regulates the concentration of urine based on body’s needs?
combined effect of ADH and Aldosterone
ENaC transports ___ ions into the cell from the lumen, leaving a _______ charge where the ___ ion exits
na
negative
k
there is a dramatic increase in ___ ion secretion in the late DCT and CD
K
K+-sparing diuretics target
ENaC
ADH or vasopressin regulates what aquaporin? where is this aquaporin located?
2
DCT and CD
other than the opening of aquaporins, ADH also regulates
urea absorption
what is the importance of urea absorption regulation by ADH
to maintain hypertonic medulla
ADH is released in response to
thirst
low Bp
in the intercalated cells, H+ is excreted across the apical membrane into the tubular fluid wia what transporters?
H+ATPase pump
or
H+/K+ ATPase exchangers
H+ secretions in the DCT and CD affect urinary pH to a minimum of
4.5
how much filtrate enters the CD on average
12 ml/min
discuss the changes to urine production when the is no ADH, average ADH and high ADH
no - 12 ml/min (o ml reabsorbed)
average - 2 ml/min (10 ml reabsorbed)
high - 0.5 ml/min (11.5 ml reabsorbed)
___% of the filtrate left with variable NaCl and H2O reabsorption at DCT and CD
10
__% of nephrons are juxtamedullary nephrons
15
salt pumps in the thick ascending limb maintains the ____mosm/L difference between the filtrate and surrounding interstitium
200
what is the anatomical arrangement of vessels so that one vessel is in the opposite direction of adjacent vessels?
countercurrent exchanger system
what is the anatomical arrangement of the LoH so that it concentrates solutes in renal medulla?
countercurrent multiplier
what is the main driving force of the countercurrent mechanism
active salt pump in thick ascending limb transports NaCl actively out of lumen and into interstitium until the interstitium is 200 mosm/L more conc than filtrate
which parts of the nephron are completely impermeable to urea
LoH
DCT
does urea concentration increase or decrease in the LoH and DCT
increases
how does ADH affect the reabsorption of urea. (include RECEPTORS)
ADH acts on collecting ducts to increase permeability of urea by promoting UTA1 and UTA3.
explain the recycling of urea.
some urea excreted goes to the medulla to increase concentration while some diffuses back into the LoH to be recycled
how much urea ends up in urine? (%)
20%
why isn’t the hypertonic interstitium washed away?
- blood flow to medulla is very low
- vasa recta capillaries operate as countercurrent exchange flow (equilibrates the medulla so net change is 0) –> goes up to 300 mosm/L
fluid movement from the ICF to the IF is _______ pressure
osmotic
fluid movement from IF to plasma is _____ pressure
hydrostatic
what is the function of RAAS
to control volume and blood pressure
what would happen if RAAS is not present
what condition is RAAS particularly important in
ischemia due to lower oxygen perfusion
hemorrhage
what is the rate limiting step of the RAAS
fall in Bp causes renin (produced by kidneys) to convert angiotensinogen (from liver) into angiotensin I. it cleaves at the leu-val bond.
what triggers the release of renin
fall in Bp
where is renin produced
juxtaglomerular cells in the kidney
what bond does renin cleave
leu - val
where is angiotensinogen produced?
liver
where is ACE located?
endothelial cells of the lung
what is the action of ACE
activated ang I by converting it to ang II (main effector)
what bond is cleaved by ACE
his - leu
what is renin first produced as
pre prorenin
where is renin stored
secretory granules until release when Bp is low
where are juxtaglomerular cells found
what type of cells are they
juxtaglomerular apparatus formed by DCT and glomerular afferent arteriole
specialised smooth muscle
the position of juxtaglomerular cells at the glomerular afferent arteriole allows it to sense
Bp and GFR
what do the macula densa cells sense
NaCl absorption
how do the macula densa cells and the juxtaglomerular cells communicate
macula densa secretions of PHE2 and PGI1
what receptor is involved when factors induce renin release (and 2nd messenger)
GsPCR and camp
what receptor is involved when factors inhibit renin release (and 2nd messenger)
GqPCR and Ca2+
use of ACE and renin inhibitors
used for patients with high Bp to decrease it
a decrease in Bp in the afferent arteriole is sensed by
baroreceptors on the juxtaglomerular cells
what factors induce renin secretion
- decrease in Bp in the afferent arteriole
- decreased NaCl reabsorption
- increase in adrenergic activity by sympathetic stimulation via B-adrenergic receptors and arteriole constriction via alpha adrenoreceptors
An increase in adrenergic activity by sympathetic stimulation via _____ receptors and arteriole constriction via _____ induces renin release.
B-adrenergic
alpha adrenoreceptors
what factors inhibit renin secretion
- increased NaCl reabsorption
- increased afferent arteriole Bp
- decreased adrenergic activity / sympathetic stimulation
- Ang II by negative feedback
what are the ang II receptors?
AT1R
AT2R
AT1R primarily mediates
cardiovascular effects of ANd II
what are AT1R receptors located
AT1Ra - blood vessels
AT1Rb - adrenal cortex and ant pit
what type of receptor is AT1R
GPCR linked to Phospholipase C with Ca+ as its second messenger as well as cAMP
use of AT1R inhibitors
treat hypertension and heart failure
where are AT2R located
fetus
neonate
function of the AT1R (5)
- tubular Na+ reabsorption in PCT by stimulating Na/H exchanger, Na/K ATPase and NA/HCO3- cotransporter
- vasoconstriction
- aldosterone release
- ADH release
- negative feedback to renin release in juxtaglomerular cells
tubular Na+ reabsorption in PCT is done by stimulating
Na/H exchanger
Na/K ATPase
NA/HCO3- cotransporter
what is the function of aldosterone
enhanced reabsorption of Na+ in the DCT –> water follows and K+ is excreted
aldosterone increases the expression of
ENaC
Na/K ATPase
effects of hyperaldosteronism
hypertension and hypokalemia
adenoma (gland - primary)
decreased renal perfusion (not in gland - secondary)
effects of hypoaldosteronism
hypotension and dehydration
addison’s (primary)
decreased renin production (SECONDARY)
what receptors are acted on by ATP
aquaporin 2
UTA 1 and 3
GFR is the main diagnostic tool to determine
renal fxn (index of renal fxn)
renal clearance is the
ml of plasma cleared of a substance in 1 min or Cs in ml/min
renal clearance is involved in measuring
the rate of excretion of a substance in relation to its plasma concentration
equation for Cs
(Us x V)/Ps
a decrease in GFR is a clinical sign of
renal disease
what is the criteria for substances that can be used to find clearance
must enter filtrate through filtration only
flows through the nephron and exits urine without being absorbed
relationship between inulin excretion and its plasma concentration
inulin excretion proportional to its plasma concentration
how does the plasma concentration of inulin affect the amount of inulin filtered
as plasma conc rises, more inulin is filtered in and ready to be excreted
the slope between rate of excretion and plasma conc represents the
clearance of inulin
is clearance dependent or independent of plasma conc?why?
independent
as plasma conc of inulin increases, clearance remains the same
how is inulin administered?
through IV
is inulin produced in the body?
NOPE
other than inulin, what substance can be used to find clearance
creatinine
what is creatinine
waste product of muscle cell’s creatine
is creatinine accurate to calculate clearance? explain.
not totally
a small quantity of creatinine is secreted into the tubule from paratubular vessels (affecting Us) but is approximately cancelled out by error in estimation of plasma concentration of creatinine (affecting Ps) which also detects another compound
Cin = Ccr =
125ml/min
formula for Ccr in males
Ccr = [(140-age) x weight (kg)] / [72 x Pcr (mg/dL)]
how does age, gender and weight affect Ccr
increased age - decreased Ccr
increased weight - increased
male - increased
formula for Ccr in females
[(140-age) x weight (kg)] / [72 x Pcr (mg/dL)] x 0.85
if someone is an athlete, how is their Ccr affected
increased
if someone if lean, how is their Ccr affected
decreased
freely filtered, not absorbed, not secreted
renal clearance =
give an example
GFR
inulin, creatinine - 125ml/min
freely filtered, fully reabsorbed, not secreted
renal clearance =
give an example
0ml/min
glucose and aa
freely filtered slightly reabsorbed, not secreted
renal clearance is
give an example
less than GFR
urea - 65 ml/min
freely filtered, not reabsorbed, fully secreted
renal clearance =
give an example
renal plasma flow
PAH - 625 ml/min
PAH asses and indicates ____ to the kidneys
blood supply
renal failure is a reduction in ____ so that kidneys cannot maintain their salt/water balance nor excrete waste
GFR
describe the onset of acute renal failure
fast onset
reversible or fatal
what type of renal failure is characterised by:
abrupt and rapid decline in renal fxn with a rapid onset caused by altered blood supply, toxins or urinary tract abnormalities
acute
edema is a consequence of what type of renal failure
acute
** salt and water retention
hyperkalemia is a consequence of what type of renal failure
acute
cardiac arrhythmias is a consequence of what type of renal failure
acute
hyperphosphatemia is a consequence of what type of renal failure
acute
Itching due to waste-product retention is a consequence of what type of renal failure
acute
what are the types of renal failure
acute
subacute
chronic
is chronic renal failure reversible?
NOPE
what type of renal failure is characterised by:
gradual irreversible loss of large numbers of functioning nephrons
chronic
in chronic renal failure, the electrolyte fluid balance is maintained at ____% of renal failure
20-30
chronic renal failure can go symptomatic until __% of the nephron is lost and is fatal after ___%
70
90
treatment of chronic renal failure
dialysis
what is the relationship of clearance of creatinine and plasma concentration of urea
inversely proportional
** used in estimating disease
how does a decrease of creatinine affect plasma conc of urea
increases
nitrogen is absorbed in our bodies from proteins in the form of ____ following fixation from bacteria in the gut
NH3
nitrogen is formed in the body by the ____ of proteins and nucleotides
catabolism
___g of nitrogen is brought in the body each day
16
this nitrogen is formed into urea in the _____ and excreted in the kidney
liver
nitrogen turnover is normally balanced where intake =
excretion
a positive nitrogen balance indicates ____
where intake is ____ than excretion
growth/ pregnancy
greater
a negative nitrogen balance indicates a catabolic state where excretion is ____ than intake
greater
does protein synthesis increase or decrease nitrogen in the body
increase
does protein catabolism increase or decrease nitrogen in the body
decrease
nitrogen turnover is dependant on the ____ turnover
aa
how much N is excreted as urea, as NH4+ and as uric acid/ creatinine (%)
85%
5%
10%
Creatine is synthesised by what amino acid in the liver?
arginine
Creatinine is formed at a constant rate of
2%
uric acid is the end product of _____ metabolism and is freely filtered in the glomerulus
purine
hyperuricemia is caused by
too much uric acid
ammonia is made from metabolism of
glutamate
urine is sterile and clear with ___% water and a pH of
93-97%
6
what does each colour of urine indicate
dark
bright yellow
red
more conc
vit D / meds
blood (disease)
what does the clarity or cloudiness of urine indicate
normal
abnormal
mucus, sperm, prostatic fluid
blood cells, bacteria
a _____ (medical test) with colour identifying degree is used in the chemical analysis of urine
dipstick
the presence of crystals in urine indicates
kidney stones
the presence of epithelial cell is urine indicates
infection/ cancer
the presence of hyaline in urine indicates
RBC
WBC
fat
average pH of blood
7.35(v) - 7.45(a)
factors that affect ph of urine (3)
- metabolism releases acid in the form of CO2
- breakdown of food –> nonvolatile acids (sulphuric and phosphoric)
- metabolic intermediates –> lactic acid –> non volatile
nitrogenous components of urine and the amount of each (%) present in urine
creatinine - 4% uric acid - 1% ammonia - 3% urea - 40% water and nacl
can non-volatile/non-carbonic acids be removed by the lungs?
NOPE
non-volatile/non-carbonic acids CANNOT be removed by the lungs. how are they removed and how much is removed per day.
bicarbonate buffer system by using HCO3-
1 mmol/day/kg
blood pH is maintained by what organs
lung and kidney
how does the lung maintain blood pH
respiratory regulation releasing Co2 as fast as it is produced
how does the kidney maintain blood pH
HCO3- (base) control to buffer acid
what are the 2 determinants of blood pH
H2CO3 (weak acid)
HCO3- (weak base)
how is blood pH calculated given the concentration of the 2 determinants of blood pH
[HCO3-] / [H2CO3]
[H2CO3] = pCO2 x ___
what does this number represent
0.03 - solubility of Co2 in the plasma
[HCO3-] is maintained at __mmol/L
24
pCO2 is maintained at ___mmHg
40
pka of H2CO3 =
6.1
pH of blood can be found by the equation
pka (H2CO3) + log [HCO3-] / [H2CO3]
where [H2CO3] = pCO2 x 0.03
for every 1 mmol of HCO3- of non volatile acid that enters the blood, how much HCO3- is removed?
1 mmol
when [H+] increases beyond the capacity of the buffer system, [HCO3-] ______ and hence HCO3- must be restored by the kidney.
decreases
where does reabsorption of HCO3- occur
80% in the PCT
20% in the DCT and LoH
describe how HCO3- is reabsorbed from filtrate
- H+ released from Na/H+ exchanger and binds to HCO3-
- H2CO3 becomes Co2 and H2O which enters the cell
- carbonic anhydrase reforms HCO3- and H+
tubular cells breakdown H2O into
H+ and OH-
H+ is secreted to the lumen through the _______ transporter and binds with ________ acids (HPO42-)
H+ATPase
non-volatile
H+ is secreted to the lumen through the _______ transporter in the CD or ____ transporter in the PCT/DCT/CD and binds with ________ acids (HPO42-)
H+ATPase
Na/H+ exchanger
non-volatile
HCO3- IS RELEASED INTO THE BLOOD THROUGH _____ CAPILLARIES
peritubular
H+ is secreted more when the pH is ___
low
titratable acid (33%) - H+ is buffered with filtrate buffers such as…. (2)
- phosphates (H2PO4- from HPO42-)
2. Creatinine (25%) in the DCT
acid with ammonia (67%) - the _____ is the main site of NH4+ synthesis and hence it is also the main site for ______ –> NH4+
PCT
H+ + NH3
pH above ____ is alkalotic
7.45
pH below ____ is acidic
7.35
which is faster: respiratory or renal adaptation
resp
does an increase in pC02 increase or decrease ventilation?
what effect does it have on the kidney?
what effect does it have on H+?
increases
kidney produces HCO3- (renal compensation)
there is also increased H+ secretion
does a decrease in HCO3-increase or decrease ventilation?
what effect does it have on the reabsorption of the HCO3-?
increases vent (body changes HCO3- into CO2) (respiratory compensation) increases reabsorption
primary defect of respiratory acidosis
increased pCO2
primary defect of meatbolic acidosis
decreased plasma HCO3- (under 24) due to an increase in other acids (other than H2CO3+)
uncontrolled diabetes, lactic acidosis, severe diarrhea and renal failure are causes of _______ acidosis
metabolic
how does insulin affect the pH (diabetic ketoacidosis)
inadequate insulin production –> decreased glucose use –> more FA metabolization and B oxidation –> ketone bodies are low in pH
how does hyperglycemia affect nerve excitability and cardiac contractility
insulin regulates K+ entry into the cell. hyperglycemia –> decreased aldosterone –> concentration K+ and salty urine –> K+ leaks out of cell and cannot re enter without insulin –> hyperkalemia –> decreases nerve excitability and increased cardiac contractility
primary defect of respiratory alkalosis
decreased pCO2
primary defect of metabolic alkalosis
increased [HCO3-]
explain the role of vomiting in metabolic alkalosis
causes H+ LOSS –> [HCO3-] remains elevated in plasma
**parietal cells secrete H+ into the lumen and HCO3- into the blood in anticipation of the reabsorption of H+ back into the blood
vomiting does not allow this to occur and hence the increase in [HCO3-] without reabsorption of H+ causes alkalosis
parietal cells secrete __ into the lumen and ____ into the blood in anticipation of the reabsorption of ___ back into the blood
H+
HCO3-
H+
how is the anion gap calculated
[unmeasured anions] = [Na+] - [Cl-] - [HCO3-] = anion gap
describe the difference between metabolic acidosis with a high anion gap and with a normal anion gap
include examples of illnesses
high - unknown anions such as lactic acid and ketone bodies reduce [HCO3-] such as in diabetes
low - such as in diarrhea, loss of HCO3-
in the kidney there is an increase in CL- due to metabolic acidosis and the anion gap shifts back to normal although acidosis is maintained
urinary epithelium is ______ epithelium
transitional
what is the ureterorenal reflex
blockage of ureter causes a build up of urine and back flow to the kidney
sympathetic innervation causes the decrease in urinary output of the kidney
what is the vesicoureteric reflux
issue with passage of ureter into the bladder causing the absence of the physiological valve –> contraction of detrusor muscle causes backflow to kidney
what are the 3 layers of muscle in the bladder
inner circular
outer longitudinal
detrusor
what characteristics of the bladder wall allow for increased volume in bladder without increasing pressure
transitional epithelium
rugae (folds in the walls)
smooth muscle plasticity
when holding in urine, what nerve is being fired?
pudendal nerve (SOMATIC)
the somatic innervation of the bladder is responsible for:
a. voiding
b. holding in urine
b
the parasympathetic innervation of the bladder is responsible for:
a. voiding
b. holding in urine
a
sympathetic innervation of the bladder is done by what nerve?
hypogastric (T10-L4)
parasympathetic innervation of the bladder is done by what nerve?
pelvic nerve (S2-S4)
somatic innervation of the bladder is done by what nerve?
S2-S4
what NT is released by hypogastric nerve, what receptors do they act on and what is the result
Noradrenaline
on B3 receptor –> inhibits detrusor muscle
on alpha 1 receptor –> stimulation of internal sphincter
what NT is released by pelvic nerve, what receptors do they act on and what is the result
ACH on M3 –> stimulates detrusor muscle
NO on M3 –> inhibits internal sphincter
what NT is released by pudendal nerve, what receptors do they act on and what is the result
ACH acts on nicotinic receptor and acts on the external sphincter
what part of the brain receives signals from the stretch receptors of the bladder?
pontine storage center
high nerve firing indicates fullness and initiates the ______ maneuver (forced expiration) due to stimulation from the _______ in the brain
pontine micturition centre
what are the 2 phases of spinal cord injury and loss of voluntary control
- areflexic - urinary retention **early
2. hyperreflexic - neurogenic detrusor overactivity **after a few weeks
describe the areflexic stage
no sensation of full bladder –> accumulation of urine –> reflux –> damage to kidney
describe the hyperreflexic stage
automatic bladder - patient has no control over the bladder or urination
the micturition reflex returns but is activated without conscious control –> overactivity of detrusor muscle
hyperreflexic stage is due to overactivity of the _____ muscle
detrusor
